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Title 

Apoptosis induced by ID6105, a new anthracycline (11-hydroxyaclacinomycin X, Hyrubicin), and its anti-tumor effects on experimental tumor models

Authors 

H S LeeJ S RyuY J JeonYoung-Soo HongJung Joon LeeS K HongT Y Kim

Publisher 

Springer Verlag (Germany)

Issue Date 

2007

Citation 

Cancer Chemotherapy & Pharmacology, vol. 60, no. 2, pp. 197-201

Keywords 

anthracyclineapoptosisbiopsied cancer cellhyrubicinID6105xenograft11 hydroxyaclacinomycin xanthracycline derivativecamptothecincaspase 3

Abstract 

A new anthracycline ID6105 (11-hydroxyaclacinomycin X, Hyrubicin), which has potent antitumor activities against a broad range of cancer cell lines, was produced by hybrid biosynthetic approach. We investigated ID6105-induced apoptosis and in vivo efficacy on experimental tumors, and also defined its optimal dosing schedule. From PARP cleavage assay and caspase-3 activation assay, we found that ID6105 can induce apoptosis in tumor cells and its ability was superior to doxorubicin. In human tumor xenograft models, ID6105 showed greater antitumor effects on SW620 and NCI-H23 than doxorubicin. The 1 mg/kg of ID6105 treatment reduced size of tumor by 93% in NCI-H23 model whereas doxorubicin (2 mg/kg) showed only 39% inhibition rate. In SW620 model, 0.3 mg/kg of ID6105 proved to be comparable to 2 mg/kg of doxorubicin. Testing with several dosing schedule such as qd10, qd5, and q4d3, we decided intravenous qd5 treatment was an optimal schedule as a dose regimen of ID6105. In conclusion, ID6105 is a potent apoptosis-inducing anthracycline and effective in treatment of tumors with qd5 dosing schedule.

ISSN 

0344-5704

Link 

http://dx.doi.org/10.1007/s00280-006-0361-z

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2017-04-19


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